Prior research in individual therapy has provided evidence that therapists are poor predictors of client outcome and often misjudge clients' perceptions of the therapeutic relationship. The focus of the current research was to conduct a similar predictive study in a group setting. Group therapists were recruited from a university counseling center and a state psychiatric hospital; 64 group members and 10 group leaders participated in the study. We tested therapist accuracy in predicting client outcome and perceived quality of therapeutic relationship. Results suggested that therapists underestimate the number of clients who deteriorate during therapy and were unable to accurately predict client perceptions of the group relationship, replicating findings from larger samples in the individual literature. Results suggest that using outcome and process measures as feedback tools may be also useful for clinicians leading groups.

We have been investigating thermoresponsive hydrogel nanoparticle composite networks to develop photopolymerized hydrogels in order to deliver drugs for prevention of restenosis after angioplasty. These composite systems can form a gel under physiological conditions and release drugs in response to temperature changes. Our novel system consisting of poly(Nisopropylacrylamide) (PNIPA) thermoresponsive nanoparticles, photo cross linker poly(ethylene glycol) diacrylate (PEGDA), and UV photoinitiator, 2-hydroxy-1-[4-(2-hydroxyethoxy) phenyl]-2-methyl-1-propanone-1-one (Irgacure 2959), would be photopolymerized in situ in the presence of UV light. The focus of this study was to evaluate the effects of a photoinitiator and UV exposure on human aortic smooth muscle cells (HASMCs). We found that exposure to UV light did not significantly affect cellular survival within doses required for photopolymerization. The photoinitiator was cytocompatible at low concentrations (≤ 0.015% w/v); however, cytotoxicity increased with increasing photoinitiator concentrations. In addition, free radicals formed in the presence of a photoinitiator and UV light caused significant levels of cell death. An antioxidant (free radical scavenger), ascorbic acid, added to the cell media significantly improved relative cell survival, but increased the hydrogel gelation time. Finally, HASMC survival when exposed to all potential cytotoxic components was also evaluated by exposing HASMCs to media incubated with our composite hydrogels. In summary, our studies show that the photoinitiator and free radicals are responsible for the cytotoxicity on HASMCs, and the addition of antioxidants can significantly reduce these harmful effects.

SUMMARY1. Single rat neurointermediate lobes were impaled on a stimulating electrode and continuously perifused with oxygenated medium. The secretion of oxytocin and vasopressin into the medium was measured by specific radio-immunoassays.2. The temporal profile of vasopressin release during a 20 min period of 13 Hz stimulation was compared with that of oxytocin. The results indicate that although the rate of secretion of both oxytocin and vasopressin declines over 20 min, the extent and time course of this fatigue is different for the two hormones. This difference could not be accounted for by differences in the rate of diffusion of released hormone from the tissue which was similar to the rate of wash-out of [14C]sucrose from the extracellular space in pre-labelled glands.3. In separate experiments glands were exposed to a prolonged period (60-70 min) of 13 Hz stimulation interrupted by brief silent periods (30 s-2 min duration). Some recovery from the fatigue of vasopressin secretion was evident after even the shortest of these silent periods.4. In further experiments glands were stimulated electrically for 18, 36, 54 and 72 s at 13 Hz: the order of presentation of the periods of stimulation was randomized between experiments. The vasopressin release rate declined markedly and progressively between 18 and 72 s. In contrast, the oxytocin release rate was relatively uniform throughout 72 s of stimulation. Thus vasopressin secretion is subject to a relatively rapid and dramatic fatigue.5. The results support the hypothesis that the phasic discharge patterns characteristic of vasopressin secreting neurones optimize the efficiency of vasopressin release from the nerve terminals in the neurohypophysis by avoiding the fatigue of stimulus-secretion coupling that accompanies continual stimulation.

The purpose of this study was to test the hypothesis that consuming a soft drink (i.e., a high-fructose, caffeinated beverage) during and following exercise in the heat elevates biomarkers of acute kidney injury (AKI) in humans. Twelve healthy adults drank 2 liters of an assigned beverage during 4 h of exercise in the heat [35.1 (0.1)°C, 61 (5)% relative humidity] in counterbalanced soft drink and water trials, and ≥1 liter of the same beverage after leaving the laboratory. Stage 1 AKI (i.e., increased serum creatinine ≥0.30 mg/dl) was detected at postexercise in 75% of participants in the Soft Drink trial compared with 8% in Water trial ( P = 0.02). Furthermore, urinary neutrophil gelatinase-associated lipocalin (NGAL), a biomarker of AKI, was higher during an overnight collection period after the Soft Drink trial compared with Water in both absolute concentration [6 (4) ng/dl vs. 5 (4) ng/dl, P < 0.04] and after correcting for urine flow rate [6 (7) (ng/dl)/(ml/min) vs. 4 (4) (ng/dl)/(ml/min), P = 0.03]. Changes in serum uric acid from preexercise were greater in the Soft Drink trial than the Water trial at postexercise ( P < 0.01) and 24 h ( P = 0.05). There were greater increases from preexercise in serum copeptin, a stable marker of vasopressin, at postexercise in the Soft Drink trial ( P < 0.02) than the Water trial. These findings indicate that consuming a soft drink during and following exercise in the heat induces AKI, likely via vasopressin-mediated mechanisms.